Tissue Culture, Cell Growth, and Analysis

Nestor, Andrea L.; Willey, James C.; Allison, David C.

doi:10.1016/b978-012655330-7/50020-4

Cited by 2 publications

(2 citation statements)

References 23 publications

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“…The SUIT-2 aneuploid cell line (derived from a male pancreatic adenocarcinoma) was a generous gift from Dr. Takeshi Iwamura (Department of Surgery, Miyazaki Medical College, Miyazaki, Japan). Each of the cell lines was grown as monolayers in DMEM (CCD34Lu and A549) or McCoy's (SUIT-2) medium containing l -glutamine, 10% FBS (Invitrogen; Carlsbad, CA), and sodium bicarbonate (Amersham Life Sciences; Arlington Heights, IL) (Nestor et al 2001). Cells were harvested from the tissue culture flasks in exponential growth phase, treated with "hypo," and dropped onto glass slides from 25 cm.…”

Section: Cell Culturementioning

confidence: 99%

Chromosomal Variations Within Aneuploid Cancer Lines

Isaka

Nestor

Takada

et al. 2003

J Histochem Cytochem.

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S U M M A R Y Aneuploid cancers exhibit a wide spectrum of clinical aggressiveness, possibly because of varying chromosome compositions. To test this, karyotypes from the diploid CCD-34Lu fibroblast and the aneuploid A549 and SUIT-2 cancer lines underwent fluorescence in situ hybridization (FISH) and DAPI counterstaining. The number of DAPI-stained and FISH-identified chromosomes, 1-22, X,Y, as well as structural abnormalities, were counted and compared using the 2 , Mann-Whitney rank sum test and the Levene's equality of variance. Virtually all of the evaluable diploid CCD-34Lu karyotypes had 46 chromosomes with two normal-appearing homologues. The aneuploid chromosome numbers per karyotype were highly variable, averaging 62 and 72 for the A549 and SUIT-2 lines, respectively. However, the A549 chromosome numbers were more narrowly distributed than the SUIT-2 karyotype chromosome numbers. Furthermore, 25% of the A549 chromosomes had structural abnormalities compared to only 7% of the SUIT-2 chromosomes. The chromosomal compositions of the aneuploid A549 and SUIT-2 cancer lines are widely divergent, suggesting that diverse genetic alterations, rather than chance, may govern the chromosome makeups of aneuploid cancers.

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Section: Cell Culturementioning

confidence: 99%

Chromosomal Variations Within Aneuploid Cancer Lines

Isaka

Nestor

Takada

et al. 2003

J Histochem Cytochem.

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“…The SUIT-2 cell line (derived from pancreatic adenocarcinoma, male) was propagated as previously described (Isaka et al, 2003). Specifically, cells were grown as a monolayer in appropriate media: DMEM (A549 and LN-18), Ham's F12K (LoVo) and McCoy's (SUIT-2) supplemented with L-glutamine, 10% FBS (Invitrogen Corporation, Carlsbad, CA), and sodium bicarbonate (Amersham Life Sciences; Arlington Heights, IL) (Nestor et al, 2001). …”

Section: Cell Culturementioning

confidence: 99%

A model for genetic complementation controlling the chromosomal abnormalities and loss of heterozygosity formation in cancer

Nestor

Hollopeter

Matsui

et al. 2007

Cytogenet Genome Res

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The relationship between the apparently random chromosomal changes found in aneuploidy and the genetic instability driving the progression of cancer is not clear. We report a test of the hypothesis that aneuploid chromosomal abnormalities might be selected to preserve cell-survival genes during loss of heterozygosity (LOH) formations which eliminate tumor suppressor genes. The LOHs and structurally abnormal chromosomes present in the aneuploid LoVo (colon), A549 (lung), SUIT-2 (pancreas), and LN-18 (glioma) cancer cell lines were identified by single nucleotide polymorphisms (SNPs) and Spectral Karyotyping (SKY). The Mann-Whitney U and chi square tests were used to evaluate possible differences in chromosome numbers and abnormalities between the cell lines, with two-tailed P values of <0.01 being considered significant. The cell lines differed significantly in chromosome numbers and frequency of structurally abnormal chromosomes. The SNP analysis revealed that each cell line contained at least a haploid set of somatic chromosomes, consistent with our hypothesis that cell-survival genes are widely scattered throughout the genome. Further, over 90% of the chromosomal abnormalities seemed to be selected, often after LOH formation, for gene-dosage compensation or to provide heterozygosity for specific chromosomal regions. These results suggest that the chromosomal changes of aneuploidy are not random, but may be selected to provide gene-dosage compensation and/or retain functional alleles of cell-survival genes during LOH formation.

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Tissue Culture, Cell Growth, and Analysis

Cited by 2 publications

References 23 publications

Chromosomal Variations Within Aneuploid Cancer Lines

Chromosomal Variations Within Aneuploid Cancer Lines

A model for genetic complementation controlling the chromosomal abnormalities and loss of heterozygosity formation in cancer

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